Effect of the Atrioventricular Relationship on Atrial Refractoriness in Humans

Atrial arrhythmias occur frequently in the setting of increased atrial size and pressure. This may result from contraction-excitation feedback. The objective of this study was to investigate the effect of alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness, and on the frequency of induction of atrial fibrillation. Twenty-seven patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory period (ARP) were measured during AV pacing at a cycle length of 400 msec and AV intervals of 0, 120, and 160 msec. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined during continuous pacing using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval was increased from 0 to 160 msec, the peak right atrial pressure decreased from 16 +/- 4 mmHg to 7 +/- 3 mmHg and the mean right atrial pressure decreased from 7 +/- 3 mmHg to 3 +/- 22 mmHg (P less than 0.001). The atrial ERP and ARP did not change with alterations in the AV interval. There was no difference in the frequency of induction of atrial fibrillation. Similar results were obtained during autonomic blockade. These findings suggests that the phenomenon of contraction-excitation feedback may not be of importance in the development of atrial arrhythmias in patients without structural heart disease.     

Diurnal Fluctuations in Human Ventricular and Atrial Refractoriness

The relative significance of the direct and indirect effects ofautonomic tone on diurnal fluctuations in human ventricular and atrial refractoriness are not well known. In this study, the circadian rhythms of ventricular and atrial effective refractory periods (ERPs) were measured by noninvasive programmed stimulation in ten patients (mean age 62 ± 10 years) who had a permanent dual chamber pacemaker for complete atrioventricular (AV) block. The ERP was measured at 4-hour intervals during spontaneous sinus rhythm with ventricular pacing (day 1)and during constant-rate dual chamber pacing (day 2). Cosinor analysis showed the ventricular ERP to have a significant diurnal rhythm in sinus rhythm (amplitude, 12 msec; 95% confidence intervals 1–24 msec) but not during constant-rate pacing (amplitude, 4 msec; 95% confidence intervals -3–12 msec). The atrial ERP had a significant rhythm at times of both spontaneous sinus rate (amplitude, 19 msec; confidence intervals 13–24 msec) and constant heart rate (amplitude, 11 msec; confidence intervals 1–21 msec) with acrophase during the sleeping hours. The increase in heart rate during dual chamber pacing resulted in a more marked decrease in the average 24-hour ERP in the ventricle than in the atrium (46 ± 9 msec vs 12 ± 6 msec, P < 0.01). Thus, refractoriness is more rate dependent in the ventricle than in the atrium, and autonomic influences on ventricular refractoriness are mainly indirect, via fluctuations in the sinus rate, but atrial refractoriness is also affected by direct neural influences and/or other rate independent factors.     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.     

Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

Atrial refractoriness and action potential duration after sudden reversal of atrioventricular sequence

To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2-8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (-40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 +/- 3 to 14 +/- 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 +/- 18 to 65 +/- 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 +/- 16 and 42 +/- 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5-10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias.     

Atrial Pressure and Experimental Atrial Fibrillation

SIDERIS, D.A., et al .: Atrial Pressure and Experimental Atrial Fibrillation . A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300–600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 ± 12.2 mmHg, mean ± SD) than maintenance of sinus rhythm (16.8 ± 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.     

Effects of Atrial Impulse Timing on AV Concealed Conduction in the Rabbit Heart

The influence of the timing of a nontrunsmitted or transmitted atrial impulse on the atrioventricular (AV) conduction time of the subsequent impulse was studied in nine isolated rabbit hearts. AV conduction curves were determined by applying the atrial extrasfimulus test. The extrasfimulus was delivered preceded or not by an interposed afrial impulse whose coupling interval with respect to the last atria] beat of a basic train was kept constant at 100, 120, 140, 160, 175, 200, 225, 250, and,300 msec. In all experiments, there was a "concealment interval," i.e., the AV effective refractory period was longer than the atrial functional refractory period, and in seven experiments was comprised between 100 and 160 msec. For any given extrastunulus coupling interval in the presence of an interposed nontransmitted atrial impulse, AV conduction time was significantly greater than in its absence; the increase was greater than the longer the nontransmifted atrial impulse coupling interval, i.e., the shorter the subsequent transmitted impulse coupling interval with respect to the previous interposed nontransmitted impulse. The AV conduction curves relating the extrastimulus AV conduction time to its coupling interval with respect to the last atrial impulse of the basic train fitted to a hyperbolic model both in the absence of the interposed atrial impulse and in its presence (mean square residual 31 ± 23 msec²). and the interposed atrial impulse modified the constants of the functions; the slope of the linear transformations was progressively more negative as the interposed atrial impulse was delayed. Furthermore, the effects of the interposed atrial impulse—transmitted or not—on AV conduction time of the subsequent impulse were qualitatively similar, their magnitude depending on the time elapsed between the two.     

Interatrial Conduction in Patients Undergoing AV Stimulation: Effects of Increasing Right Atrial Stimulation Rate

To evaluate the frequency of spontaneous or rate dependent interatrial blocks, the interatrial conduction time (IACT) was studied on 100 consecutive patients (mean age 78.3 ±7.8 years) during a transvenous dual chamber pacemaker implant. The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the unipolar right atrial signal to the ID of the left atrial signal recorded in a bipoiar way by an esophageal lead. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID, when the atrium was paced at a slightly higher rate than the spontaneous rate and during incremental atrial pacing. From these measurements, the maximum increase ofPIACT (MIPIACT) was deduced. In this elderly population, the PIACT was similar (117 ± 26.9 msec) to the data in the literature. However, there were large interindividual variations that were also found in SIACT. We found a close correlation between SIACT and PIACT (P < 0.0001). PIACT was on average 50 msec longer than SIACT. SIACT increased with age (P < 0.03). The MIPIACT was 15.3 ± 15.2 msec. In the majority of patients, the MIPIACT was > 10 msec, and even reached 90 msec in one patient. MIPIACT was longer in patients with a PIACT exceeding 110 msec (P < 0.004). Based on IACT alone, the AV interval must be lengthened on average by 50 msec when changing from atrial tracking-ventricular pacing to atrial pacing-ventricular pacing, but large individual differences must be kept in mind. Elderly people should probably have a longer AV delay.     

Evaluation of Transesophageal Atrial Pacing Stethoscope in Adult Surgical Patients Under General Anesthesia

Sinus bradycardia (SB) and atrioventricular functional rhythm (AVJR) commonly cause circulatory insufficiency in anesthetized surgical patients. Treatment is usually with drugs, which can be ineffective or have adverse effects. Cardiac pacing might be preferred, but the transvenous or epicardial routes are too invasive for routine use, and transcufaneous pacing fails to preserve atrial transport function, Transesophageal atrial pacing (TAP) lacks these disadvantages, yet inavailability of inexpensive products has prevented more widespread use. Therefore, a pacing esophageal stethoscope (PES) fabricated by addition of bipolar electrodes to disposable esophageal stethoscopes routinely used for intraoperative monitoring, was evaluated in 100 anesthetized adults. TAP thresholds (10-msec pulses) and hemodynamic effects of TAP as treatment for incidental SB (< 60 beats/mm) or AVJR were determined. Minimum TAP thresholds (mean ± standard error) in 48 males were 7.3 ± 0.3 mA and in 51 females were 8.5 ± 0.4 mA. Corresponding inferior alveolar ridge-to-electrode distances were 32.5 ± 0.2 and 30.4 ± 0.2 cm. For 48 patients with SB ± 60 beats/mm (54 ± 1 beats/min), TAP (81 ± 1 ppm) produced average 15, 11, and 14 mmHg increases in systolic, diastolic, and mean arterial pressure, respectively (P < 0.001). For 11 patients with AV/R (71 ± 5 beats/mm), TAP (92 ± 3 ppm) produced average 23 and 15 mmHg increases in systolic and mean arterial pressure, respectively (P < 0.05). There were no apparent complications of TAP. TAP with a PES appears practical, safe, and effective for prophylaxis and treatment of SB or AV/R in anesthetized surgical patients.     

Retrograde Supernormal Conduction, Gap Phenomenon in Concealed Accessory Atrioventricular Pathways

We present four patients with the Wolff-Parkinson-White syndrome who exhibited retrograde supernormal conduction or gap phenomenon in concealed accessory pathways. In the first patient, ventricular extrastimulus testing revealed retrograde block at the coupling interval of 520 msec and reappearance of conduction at the coupling interval of 370 msec. In a second patient, 1:1 retrograde conduction was not present but supernormal conduction was demonstrated at coupling intervals of 360 msec to 310 msec during the ventricular extrastimulus testing when the basic drive consisted of atrioventricular (AV) simultaneous pacing. In a third patient, ventricular extrastimulus testing demonstrated retrograde conduction through the accessory pathway only at coupling intervals of 400 msec to 360 msec. In a fourth patient, retrograde block occurred at the coupling interval of 340 msec and retrograde "slow" conduction reappeared at coupling intervals of 300 msec to 250 msec (gap phenomenon) only when the basic drive consisted of AV simultaneous pacing. Thus, concealed accessory pathways may exhibit retrograde supernormal conduction or gap phenomenon. Ventricular extrastimulus testing consisting of AV simultaneous pacing during the basic drive may facilitate demonstration of these unusual properties.     

Change of Atrial Refractory Period after Short Duration of Rapid Atrial Pacing: Regional Differences and Possible Mechanisms

It is unknown whether there are regional differences in the cimnge of atrial effective refractory period (EBP) after a short duration of rapid atriai pacing. Furthermore, the effects of calcium channel and potassium channel on this phenomenon have not been extensively investigated. In opened-chest dogs, the endocardial monophasic action potential duration at 90% repolarization (APD₉₀) from the right atrial appendage, and ERP from seven atrial sites were measured before and after rapid atrial pacing at 800 beats/min for 30 minutes. Both atrial ERP and APD₉₀ significantly shortened after rapid atrial pacing. The postpacing atria EBP and APD₉₀ shortening persisted for 1.19 ± 3 and 123 ± 4 seconds after cessation of pacing, respectively. There was no significant difference in the magnitude or recovery course of atrial ERP shortening after pacing among the seven atrial sites. Pretreatment with nicorandil and d-sotalol had no effects on the magnitude or recovery course of atrial EBP shortening after pacing. However, the degree of ERP and APD₉₀shortening after pacing was significantly atten uated in the verapamil and ryanodine groups; furthermore, the recovery of ERP and APD₉₀ after cessation of pacing was faster in the two groups. In conclusion, shortening of atrial EBP induced by short-duration rapid atrial pacing was uniform in both atria. Both the adenosine triphosphatase (ATP) dependent potassium current and rapid component of the delayed rectifier did not significantly influence this phenomenon, but both the verapamil and ryanodine could significantly attenuate the degree of atrial ERP and APD₉₀ shortening.     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Hemodynamic Responses to Rapid Pacing: A Model for Tachycardia Differentiation

The hemodynamic responses to rapid atrial and ventricular pacing were examined in 10 closed-chest anesthetized dogs in an attempt to distinguish hemodynamically stable from unstable tachycardias. Pressure monitoring catheters were placed in the femoral artery, right atrium, and right ventricle to measure mean arterial pressure, mean right atrial pressure, and mean right ventricular pressure at baseline heart rate and after rapid high right atrial and right ventricular apex pacing. Pressures recorded during rapid pacing (average of the pressures at 30 and 60 seconds of pacing) at pacing rates of 180, 250, and 280/minute were compared to those recorded initially at baseline heart rates. Rapid right ventricular apex pacing resulted in significant increases in mean right atrial pressure (from 6 ± 1 mmHg (mean ± standard error) to 12 ± 1 mmHg, a 100% increase, P < 0.001) and mean right ventricular pressure (from 11 ±1 mmHg to 16 ± 1 mmHg, a 45% increase, p < 0.02) with marked hemodynamic compromise (mean arterial pressure decreased from 85 ± 6 mmHg to 50 ± 6 mmHg, a 41% decrease, P < 0.01). These parameters remained stable (no statistically significant difference from baseline) during high right atrial pacing. In half of the dogs high right atrial pacing at rates 250 resulted in atrioventricular Wenckebach. Thus, it is concluded that mean right atrial pressure and mean right ventricular pressure may be useful in distinguishing hemodynamically significant tachycardias, and in the future design of antitachycardia devices.     

Quantitative Relationship Between Atrial Refractoriness and the Dispersion of Refractoriness in Atrial Vulnerability

We investigated the quantitative relationship between the atrial refractory period and the dispersion of refractoriness with respect to atrial vulnerability in 19 adult mongrel dogs. The atrial effective refractory period (AERP) was measured at the sinus node area (SNA), the low posterior right atrium (LRA), and the distal coronary sinus. The study was performed under the following conditions: (1) control status; (2) hypothermia (30°C); (3) vagus nerve stimulation; and (4) a combination of (2) and (3). The subjects were separated into two groups: atrial fibrillation (AF) (+) group (n = 23), which developed AF by atrial extrastimulus due to increased vulnerability, and AF (−) group (n = 39), which did not develop AF. The mean AERP was 97 ± 23 msec (mean ± SD) in the AF (+) group and 124 ± 23 msec in the AF (−) group, with a significantly shorter refractory period seen in the former (P < 0.001). The dispersion of refractoriness was 59 ± 24 msec in the AF (+) group and 29 ± 18 msec in the AF (−) group, with a significant increase noted in the former (P < 0.001), On X-Y coordinates (where X denotes the AERP, and Y denotes the dispersion of refractoriness) the data from the AF (+) group were clustered in the upper left region of the graph while the data from the AF (−) group were clustered in the lower right region. These two groups were separated by a linear equation of Y = 0.86X - 57 with a predictability of 90.3%. No difference in the time from SNA stimulation to LRA excitation was found between the groups. On the basis of these results, we suggest that increased atria) vulnerability can be predicted from an analysis of the quantitative relationship between the atrial refractory period and the dispersion of refractoriness.     

Pacemaker Syndrome in a Patient with DDD Pacemaker for Long QT Syndrome

A patient with long QT syndrome was treated with beta blockers and had a permanent DDD pacemaker implanted. The lower rate was set to 85 beats/min because this provided the best shortening of QT interval at the lowest paced heart rate. The atrioventricular (AV) delay was programmed to 250 msec to allow native AV conduction. Patient returned complaining of symptoms suggestive of pacemaker syndrome. ECG during one of these episodes showed AV sequential pacing. Doppler echocardiography of hepatic vein flow suggested atrial contraction against a closed tricuspid valve. Endocardial electrogram telemetry demonstrated ventriculoatrial (VA) conduction with the retrograde atrial electrogram falling within the atrial refractory period and thus was not sensed. The following atrial stimulus did not capture because of the atrial refractoriness. Ventricular pacing proceeded after the programmed AV delay. Reprogramming the AV delay to 200 msec restored AV synchrony by allowing the atrial stimulus to capture by placing it outside of the refractory period of the atrium. No further symptoms reported during six months of follow-up.     

Atrial Septal Pacing to Synchronize Atrial Depolarization in Patients with Delayed Interatrial Conduction

The current method of pacing the right atrium from the appendage or free wall is often the source of delayed intraatrial conduction and discoordinate left and right atrial mechanical function. Simultaneous activation of both atria with pacing techniques involving multisite and multilead systems is associated with suppression of supraventricular tachyarrhythmias and improved hemodynamics. In the present study we tested the hypothesis that pacing from a single site of the atrial septum can synchronize atrial depolarization. Five males and two females (mean age 58 ± 6 years) with drug refractory paroxysmal atrial fibrillation (AF) were studied who were candidates for AV junctional ablation. All patients had broad P waves (118 ± 10 ms) on the surface ECG. Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle, and distal coronary sinus (CS) were recorded. The atrial septum was paced from multiple sites. The site of atrial septum where the timing between HRA and distal CS (d-CS) was ≤ 10 ms was considered the most suitable for simultaneous atrial activation. An active fixation atrial lead was positioned at this site and a standard lead was placed in the ventricle. The interatrial conduction time during sinus rhythm and AAT pacing and the conduction time from the pacing site to the HRA and d-CS during septal pacing were measured. Atrial septal pacing was successful in all patients at sites superior to the CS os near the fossa ovalis. During septal pacing the P waves were inverted in the inferior leads with shortened duration from 118 ± 10 ms to 93 ± 7 ms (P < 0.001), and the conduction time from the pacing site to the HRA and d-CS was 54.3 ± 6.8 ms and 52.8 ± 2.5 ms, respectively. The interatrial conduction time during AAT pacing was shortened in comparison to sinus rhythm (115 ± 18.9 ms vs 97.8 ± 10.3 ms, P < 0.05). In conclusion, simultaneous activation of both atria in patients with prolonged interatrial conduction time can be accomplished by pacing a single site in the atrial septum using a standard active fixation lead placed under electrophysiological study guidance. Such a pacing system allows proper left AV timing and may prove efficacious in preventing various supraventricular tachyarrhythmias.     

Electrophysiological Demonstration of Anterograde Concealed Conduction in Accessory Atrioventricular Pathways Capable Only of Retrograde Conduction

Anterograde concealed conduction into the concealed accessory atrioventricular (AV) pathway has been postulated to be one of the factors preventing the reciprocating process via the accessory pathway in patients with the concealed Wolff-Parkinson-White(WPW) syndrome but its presence has not been documented. To demonstrate the occurrence of anterograde concealment, 12 patients with the concealed WPW syndrome were selected for study. A pacing protocol was designed in which the retrograde conduction of the ventricular extrastimulus over the accessory pathway was assessed during ventricular pacing aione (conventional method) and during the AV simultaneous pacing (simultaneous method); the results were then compared. When the high right atrium was simultaneously paced, the effective refractory period of the concealed accessory pathway shortened as compared with the conventional method in five of 12 patients (from 341.7 ± 110.8 to 312.5 ± 108.2 msec, n = 12), whereas, it decreased in all patients studied when the coronary sinus near the accessory pathway was simultaneously paced (from 375.7 ± 135.0 to 287. ± 116.1 msec, n = 7). These results demonstrate that the AV simultaneous pacing frequently shortens the refractoriness of the concealed accessory AV pathway and such facilitation seems to he well explained by the probable anterograde concealment in it and peeling back of the refractory barrier.     

Relationship Between Interatrial Conduction Times and Left Atrial Dimension in Patients Undergoing Atrioventricular Stimulation

Interatrial conduction time (IACT) and left atrial dimension (LAD) were determined in 75 patients (41 males, 34 females, mean age 78.2 ± 7,9 years) undergoing atrioventricular (AV) stimulation. The LAD was measured by M mode echocardiography as the distance between the posterior aortic wall and the posterior left atrial wall. The IACT was determined during a transvenous dual chamber pacemaker implant done under local anesthesia (lidocaine). The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the right atrium recorded in a unipolar mode (unipolar J-shaped had positioned in the right appendage) to the ID of the left atrium (bipolar esophageal lead, left atrial positive deflection equal to the negative one) during sinus rhythm. The right atrium then was paced at a rate slightly greater than the spontaneous one. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID. The PIACT was also measured during incremental right atrial pacing (10 beats/min step increase to 180 beats/min) and, from these measurements, the maximum increase of PIACT (MIPIACT) was deduced. The LAD was measured at 39.5 ± 8.7 mm, SIACT at 70.3 ± 24.8 msec, PIACT at 118.8 ± 27.9 msec, and MIPIACT at 16.5 ± 16.4 msec. We found highly significant relationships between SIACT and LAD(P = 0.0006, r - 0.39), PIACT and LAD (P = 0.0001, r = 0.45), and MIPIACT and LAD (P = 0.0006, r = 0.38). We also noted that the LAD was greater in patients in whom MIPIACT was >10 msec than in patients in whom the MIPIACT was negligible (P < 0.002). However, the “r” values indicate that IACT is probably determined by multiple factors, and LAD appears to be one of the most important. Thus, we demonstrated the existence of highly significant relationships between the LAD determined by M mode echocardiography and the IACT when sensing and pacing the right atrium. We also demonstrated that the LAD was greater in patients in whom PIACT increased by an appreciable duration during fast atrial pacing. These results must be kept in mind when choosing a mode of stimulation and determining the AV delay (dual chamber pacemaker), particularly in patients with left atrial enlargement in whom the contribution of the atrial contraction and its timing are hemodynamically determinant.     

Rate Adaptive Atrial Pacing in the Bradycardia Tachycardia Syndrome

In 42 patients (26 men, 16 women; mean age 69 ± 10 years), who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome, chronotropic response and AV conduction with rapid atrial pacing during exercise were studied. Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval ≤ 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest with an AAI pacing rate of 5 beats/min above the sinus rate (SQ-R+5), and at the end of exercise with 110 beats/min (SQ-E110). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol with the pacemakers being programmed to AAI with a fixed rate of 60 beats/min. Chronotropic incompetence was defined as peak exercise heart rate: (1) < 100 beats/min; (2) < 75% of the maximum predicted heart rate; or (3) the heart rate at half the maximum workload < 60 + 2 beats/min per mL O₂/kg per minute (calculated O₂ consumption). During exercise, one patient developed atrial fibrillation. Chronotropic incompetence was present in 71 % (29/41) of the patients according to definition 2, and in 76% (31/41) according to definition 1 or 3. Ten out of 41 patients (24%) exhibited a second-degree AV block with atrial pacing at 110 beats/min at the end of exercise. Only 9 out of the remaining 31 patients (29%) showed a physiological adaptation of the SQ-E110, and 21 patients (68%) exhibited a paradoxical increase of the SQ interval with rapid atrial pacing at the end of exercise as compared to the SQ-R+5. These observations indicate that the pacing system to be used in most patients paced and medicated for the bradycardia tachycardia syndrome should be dual chamber, and the option of rate adaptation should be considered.